1
Q
What is the primary difference between the mechanism of action for Lipid-soluble vs. Water-soluble hormones?
A
Lipid-soluble (Steroids, Thyroid) have intracellular receptors and affect DNA; Water-soluble (Peptides, Catecholamines) have cell surface receptors and usually require second messengers.
2
Q
What is the ‘Wolf-Chaikoff mechanism’ regarding the Thyroid?
A
An adaptive decline in the utilization of iodine when there is an excess of iodine present.
3
Q
How does T3 compare to T4 in terms of potency and secretion?
A
T3 is five times as potent as T4, but T4 makes up 90% of the released product.
4
Q
What are the signs of a Thyroid Storm?
A
High fever, tachycardia, delirium, chest pain, dyspnea, palpitations, weight loss, diarrhea, and abdominal pain.
5
Q
What is the preferred treatment sequence for Thyroid Storm?
A
Oxygen/Fluids, Hypothermic measures, Steroids (for adrenal deficiency), Iodine (decrease T4 output), Beta-blockers, and Tapazole/PTU (block synthesis).
6
Q
What are the airway concerns following a subtotal thyroidectomy?
A
Hematoma causing tracheal compression, or bilateral recurrent laryngeal nerve injury causing vocal cord paralysis (cords flap together causing obstruction).
7
Q
What is Chvostek’s sign and what does it indicate?
A
Spasm of the mouth/nose/eye when tapping over the facial nerve; indicates Hypocalcemia (Hypoparathyroidism).
8
Q
What is Trousseau’s sign and what does it indicate?
A
Carpopedal spasm (claw hand) manifested when a BP cuff is inflated; indicates Hypocalcemia.
9
Q
What is the immediate treatment for severe Hypocalcemia with tetany?
A
IV Calcium Gluconate.
10
Q
What hormones are secreted by the Adrenal Cortex?
A
Mineralocorticoids (Aldosterone), Glucocorticoids (Cortisol), and Adrenal Androgens.
11
Q
What is the hallmark of Pheochromocytoma?
A
A catecholamine-secreting tumor (usually adrenal medulla) causing paroxysmal hypertension.
12
Q
What is the ‘Classic Triad’ of symptoms for Pheochromocytoma?
A
Diaphoresis, Tachycardia (Palpitations), and Headache.
13
Q
What is the crucial order of drug therapy for Pheochromocytoma prior to surgery?
A
Alpha blockade must be established before Beta blockade. (Alpha blockers: Phenoxybenzamine/Prazosin; Beta blockers: Propranolol).
14
Q
Why must Alpha blockade precede Beta blockade in Pheochromocytoma management?
A
Beta blockade alone leaves alpha-adrenergic effects unopposed, potentially worsening hypertension.
15
Q
What anesthesia drugs should be avoided in Pheochromocytoma patients?
A
Drugs that stimulate the SNS, Droperidol (may provoke catecholamine release), and potentially Succinylcholine (due to histamine release/fasciculations).
16
Q
What is Addison’s Disease?
A
Primary adrenocortical insufficiency (deficiency of cortical hormones, specifically cortisol and aldosterone).
17
Q
What are the physical signs of Cushing’s Syndrome (Hypercortisolism)?
A
Central obesity, muscle wasting, striae, hyperglycemia, hypertension, and hirsutism.
18
Q
What is the cause of Diabetes Insipidus (DI)?
A
Deficiency of ADH (Antidiuretic Hormone), leading to excessive thirst and large volumes of dilute urine.
19
Q
What is SIADH?
A
Syndrome of Inappropriate Antidiuretic Hormone: Excessive ADH secretion causing fluid retention and dilutional hyponatremia.
20
Q
What is the Somogyi effect (implied by ‘rebound’ concepts in diabetes)?
A
Not explicitly defined in text, but hypoglycemia is noted as the most dangerous acute problem in T1DM treatment. Note: Text mentions insulin levels dropping and glucagon working to release glucose.
21
Q
How does Diabetes Mellitus affect the airway and intubation (Stiff Joint Syndrome)?
A
Glycosylation of collagen leads to limited joint mobility (prayer sign), potentially making intubation difficult.
22
Q
What is the concern with Autonomic Neuropathy in diabetic patients undergoing anesthesia?
A
It causes gastroparesis (aspiration risk), orthostatic hypotension, resting tachycardia, and potential painless myocardial infarction.
23
Q
Why are volatile anesthetics theoretically concerning in diabetic patients?
A
They may impair the release of insulin in response to glucose administration.
24
Q
What are the ECG changes associated with Hyperkalemia?
A
Peaked T waves, prolonged PR interval, loss of P wave, widening QRS complex.
25
What is the acute treatment for Hyperkalemia?
Calcium Gluconate (cardiac protection), Glucose/Insulin, Bicarbonate, Hyperventilation, Diuretics, Kayexalate.
26
What is the most common cause of Hypernatremia?
Total body water deficit (not usually an excess of total body sodium).
27
How does Acidosis affect serum Potassium levels?
Acidosis favors the passage of potassium from intracellular to extracellular space (Hyperkalemia).
28
What is the pathophysiology of Multiple Sclerosis (MS)?
Immune-mediated demyelination and axonal damage in the CNS (white matter inflammation).
29
How does MS affect the response to neuromuscular blockers?
Succinylcholine causes prolonged response and hyperkalemia (avoid it); Resistance to Non-depolarizers.
30
What is the pathophysiology of Myasthenia Gravis (MG)?
Chronic autoimmune disease of the neuromuscular junction (NMJ) attacking Acetylcholine receptors.
31
How does MG affect the response to neuromuscular blockers?
Resistant to Succinylcholine (requires higher dose but lasts longer D/T anticholinesterase treatment (prevents plasma cholinesterases from breaking it down); Increased sensitivity to Non-depolarizers (requires much lower dose D/T fewer receptors).
32
What is CREST syndrome in Scleroderma?
Calcinosis, Raynaud’s phenomenon, Esophageal dysfunction, Sclerodactyly, Telangiectasias.
33
What are the anesthetic airway concerns for Scleroderma?
Decreased mandibular motion and narrowing of oral aperture (taut skin) make intubation difficult.
34
Why is pulmonary hypertension a concern in Scleroderma?
Intimal fibrosis of pulmonary artery walls is common; cardiac evaluation is required pre-op.
35
What specific complication is associated with rapid correction of Hyponatremia?
Central Pontine Myelinolysis (implied by 'Restoration of electrolytes must be gradual').
36
What is the 'Prayer Sign' in diabetes?
Inability to press palms flat together due to stiffness of the hands/neck/cords (Stiff Joint Syndrome).
37
What is the primary anesthetic risk for a patient with a mediastinal mass (e.g., retrosternal thyroid)?
Airway obstruction or tracheal compression.
38
What is the difference between Primary and Secondary endocrine disorders?
Primary is dysfunction of the target gland (e.g., Thyroid); Secondary is dysfunction of the pituitary gland.
39
How does Aldosterone affect the kidneys?
Increases reabsorption of Sodium (and water) and excretion of Potassium.
40
What are the '5 H's' of Pheochromocytoma symptoms?
Hypertension, Headache, Hyperhidrosis (sweating), Hypermetabolism, Hyperglycemia.
41
What is the 'Prayer Sign' and what can it affect?
A sign (associated with metabolic syndrome/diabetes) where stiffness of collagen prevents pressing palms flat together; it can also affect the stiffness of the neck and vocal cords.
42
Name the major glands of the Endocrine System listed in the presentation.
Hypothalamus, Posterior Pituitary, Anterior Pituitary, Thyroid, Parathyroids, Adrenals, Pancreatic islets, Ovaries, and Testes.
43
What hormones are released or inhibited by the Hypothalamus?
Corticotropin-releasing hormone (CRH), Thyrotropin-releasing hormone (TRH), Growth hormone-releasing hormone (GHRH), Gonadotropin-releasing hormone (GnRH), and Somatostatin (which inhibits GH and TSH).
44
What hormones are released by the Anterior Pituitary?
Growth Hormone (GH), Adrenocorticotropic hormone (ACTH), Thyroid stimulating hormone (TSH), Follicle stimulating hormone (FSH), Luteinizing hormone (LH), and Prolactin.
45
What two hormones are released by the Posterior Pituitary?
Antidiuretic Hormone (ADH) and Oxytocin.
46
What are the three classes of hormones produced by the Adrenal Cortex?
1. Mineralocorticoids (e.g., Aldosterone), 2. Glucocorticoids (e.g., Cortisol), 3. Adrenal Androgens (e.g., DHEA).
47
What is the function of Mineralocorticoids (Aldosterone) from the Adrenal Cortex?
Affects sodium absorption and the loss of potassium by the kidney.
48
What are the functions of Glucocorticoids (Cortisol) from the Adrenal Cortex?
Affects metabolism, regulates blood sugar, affects growth, has anti-inflammatory action, and decreases the effects of stress.
49
What hormones are released by the Adrenal Medulla?
Epinephrine and Norepinephrine (which serve as neurotransmitters for the sympathetic system).
50
What hormones are released by the Thyroid's Follicular cells and what is their function?
Triiodothyronine (T3) and Thyroxine (T4); they increase BMR, increase bone/calcium turnover, increase response to catecholamines, and are needed for fetal G&D.
51
What hormone is released by the Thyroid C cells and what is its function?
Calcitonin; it lowers blood calcium and phosphate levels.
52
What hormone does the Parathyroid release and what does it do?
Parathyroid hormone (PTH); it regulates (increases) serum calcium.
53
What are the key hormones from the Pancreatic Islet cells and their functions?
Insulin (promotes glycogen storage), Glucagon (stimulates glycogenolysis - breakdown of glycogen), and Somatostatin (decreases intestinal absorption of glucose).
54
What endocrine-related substances are produced by the Kidney?
1, 25 dihydroxyvitamin D (stimulates Ca absorption), Renin (activates RAAS), and Erythropoietin (increases RBC production).
55
What is the function of Progesterone from the ovaries?
Important in the menstrual cycle and *maintains pregnancy* (prevents contractions).
56
What hormones does the Thymus release and what is their function?
Thymosin and Thymopoietin; they affect the maturation of T lymphocytes.
57
What hormone does the Pineal gland release and what does it affect?
Melatonin; affects sleep, fertility, and aging.
58
What conditions can Eosinophilic pituitary tumors cause?
Gigantism (if early in life) or Acromegaly (if later in life).
59
What condition can Basophilic pituitary tumors cause?
Cushing's syndrome with features of hyperadrenalism (truncal obesity, amenorrhea, osteoporosis).
60
What do Chromophobic pituitary tumors (90% of pituitary tumors) present with?
Lowered BMR, obesity, somnolence, scant hair, low body temp, headaches, and visual changes.
61
What does Growth hormone deficiency in childhood result in?
Primary dwarfism.
62
What is Diabetes Insipidus (DI)?
A deficiency of ADH (Antidiuretic Hormone) leading to excessive thirst and large volumes of *dilute* urine.
63
What is Nephrogenic DI?
A failure of the *renal tubules* to respond to ADH. Can be related to hypokalemia, hypercalcemia, or medications (Lithium).
64
What is the characteristic urine specific gravity in Diabetes Insipidus?
Very low: 1.001 to 1.005.
65
What is the Fluid Deprivation Test for DI?
Withhold fluids for 8-12 hours. Inability to slow urinary output and concentrate urine is diagnostic. Stop the test if the patient becomes tachycardic or hypotensive.
66
What is the primary pharmacologic treatment for DI?
DDAVP (desmopressin), an ADH analog, given intranasally or IM.
67
What is SIADH?
Syndrome of Inappropriate ADH: *Excessive* ADH secretion, causing fluid *retention* and a *dilutional hyponatremia*.
68
What are common non-endocrine causes of SIADH?
Bronchogenic carcinoma (small cell lung cancer), head injury, brain surgery, CNS tumors/infections, or medications (Vincristine, TCAs, Thiazide diuretics).
69
How is SIADH managed?
Eliminate the cause, give diuretics (e.g., Lasix), *fluid restriction*, I&O, and daily weights.
70
How should electrolytes be restored in a patient with SIADH?
Gradually, to prevent central pontine myelinolysis. May use 3% hypertonic saline in conjunction with Lasix for severe cases.
71
What element is essential for the synthesis of thyroid hormones T3 and T4?
Iodine.
72
What is the Wolf-Chaikoff mechanism?
An adaptive decline in thyroid hormone production caused by the ingestion of a large amount of iodine.
73
How does T3 potency compare to T4?
T3 is five times as potent as T4.
74
What is the T3 resin uptake test useful for?
Evaluating thyroid hormone levels in patients who have recently received a diagnostic or therapeutic dose of iodine.
75
On a radioactive iodine uptake test, what findings suggest hyperthyroidism vs. hypothyroidism?
Hyperthyroidism: High uptake. Hypothyroidism: Low uptake.
76
On a thyroid scan, what do 'hot' and 'cold' areas indicate?
'Hot' areas = increased function; 'Cold' areas = decreased function (higher suspicion for malignancy).
77
What nerve is at high risk of injury during thyroid surgery and must be monitored?
The recurrent laryngeal nerve.
78
What is the most common cause of hypothyroidism?
Hashimoto's thyroiditis (an autoimmune disease).
79
What medications are known to cause hypothyroidism?
Lithium, iodine compounds, and antithyroid medications.
80
What is myxedema?
The extreme form of hypothyroidism, involving the accumulation of mucopolysaccharides in subcutaneous and interstitial tissues. Can progress to shock.
81
What are the classic signs/symptoms of hypothyroidism?
Fatigue, hair loss, dry skin, brittle nails, numbness/tingling, amenorrhea, weight gain, decreased heart rate & temp, cognitive changes, elevated cholesterol, constipation.
82
What is the preferred pharmacologic agent for hypothyroidism?
Levothyroxine (Synthroid). Dosage is based on TSH levels.
83
What cardiac risk can occur when initiating thyroid replacement (Levothyroxine) in a patient with CAD?
Angina, as it enhances the effects of cardiovascular catecholamines. Treatment should be started at a low dose.
84
What is the extreme form of hyperthyroidism (thyrotoxicosis)?
Grave's disease.
85
What are the classic manifestations of hyperthyroidism?
Nervousness, irritability, apprehension, palpitations, heat intolerance, skin flushing, tremors, and possibly exophthalmos (bulging eyes).
86
What physical assessment findings are common in hyperthyroidism?
An enlarged thyroid gland, and possibly a thyroid thrill and/or bruit.
87
What are the typical lab findings in primary hyperthyroidism?
Decreased TSH, increased free T4, and an increased radioactive iodine uptake.
88
What are the three main management strategies for hyperthyroidism?
1. Radioactive iodine, 2. Antithyroid medications, 3. Surgery. (Beta-blockers are used for symptomatic control).
89
What are the signs and symptoms of a Thyroid Storm?
High fever, extreme tachycardia, delirium, chest pain, dyspnea, palpitations, weight loss, diarrhea, and abdominal pain.
90
How is a thyroid storm managed?
Oxygen, IV fluids w/ dextrose, hypothermic measures, steroids (for shock/adrenal deficiency), iodine (to decrease T4 output), beta-blockers, and antithyroid meds (Tapazole/PTU).
91
Name the common antithyroid medications.
PTU (propylthiouracil), Tapazole (methimazole), Sodium Iodide, SSKI (saturated solution of potassium chloride), and Dexamethasone.
92
What is SSKI (saturated solution of potassium chloride) used for and what is a side effect?
Used pre-operatively to suppress thyroid hormone release and decrease the vascularity of the thyroid gland. It can stain teeth.
93
What medications are given before a subtotal thyroidectomy?
PTU (until S/S of hyperthyroidism disappear) and Iodine (to decrease vascularity).
94
What is the function of Parathormone (PTH)?
It maintains (increases) sufficient serum calcium levels.
95
What are the two main complications of hyperparathyroidism?
1. Bone decalcification and 2. Development of renal calculi (kidney stones).
96
What is the most common cause of *secondary* hyperparathyroidism?
Chronic renal failure, which causes excess phosphorus retention (leading to increased parathormone secretion).
97
What are the manifestations of hyperparathyroidism?
Apathy, fatigue, muscle weakness, N/V, constipation, hypertension, cardiac dysrhythmias, psychosis, renal lithiasis, bone pain, peptic ulcers, pancreatitis.
98
What are the key diagnostic findings for hyperparathyroidism?
Persistent elevated serum calcium levels and an elevated serum parathormone level.
99
What is the recommended treatment for primary hyperparathyroidism?
Surgical removal of the gland(s).
100
What diuretic should be *avoided* in hyperparathyroidism and why?
Thiazide diuretics, as they *decrease* the renal excretion of calcium, worsening the hypercalcemia.
101
What major complication should be watched for post-surgically after a parathyroidectomy?
Tetany (from hypocalcemia), as well as dysrhythmias and hypotension.
102
What serum calcium level defines a hypercalcemic crisis?
Greater than 15 mg/dL.
103
How is a hypercalcemic crisis treated?
Hydration, loop diuretics (to promote Ca excretion), phosphate therapy, and Calcitonin or Mithramycin (to decrease serum calcium levels quickly).
104
What is the most common cause of hypoparathyroidism?
Iatrogenic (accidental removal) following thyroid surgery, parathyroid surgery, or radical neck surgery.
105
What is the pathophysiology of hypoparathyroidism?
A deficiency of parathormone results in *increased* bone phosphate and *decreased* blood calcium levels.
106
What is the hallmark clinical manifestation of hypoparathyroidism?
Tetany: hypertonic muscle contractions, numbness, tingling, cramps, laryngeal spasm, bronchospasm, carpopedal spasm, seizures.
107
What is Chvostek's sign and what does it indicate?
Tapping over the facial nerve causes a spasm of the mouth, nose, and eye. It indicates hypocalcemia.
108
What is Trousseau's sign and what does it indicate?
Inflating a BP cuff causes carpopedal spasm (flexion of the wrist and thumb). It indicates hypocalcemia.
109
What is the immediate management for acute tetany from hypoparathyroidism?
IV Calcium Gluconate (must be kept at the bedside).
110
What is a pheochromocytoma?
A (usually benign) tumor originating from the chromaffin cells of the adrenal medulla that secretes catecholamines (epinephrine, norepinephrine).
111
What are the 'classic triad' of symptoms for pheochromocytoma?
Headache, Diaphoresis (sweating), and Palpitations (tachycardia), associated with severe hypertension.
112
What are the '5 H's' associated with pheochromocytoma?
Hypertension, Headache, Hyperhidrosis, Hypermetabolism, and Hyperglycemia.
113
What are the conclusive diagnostic tests for pheochromocytoma?
24-hour urine collection for catecholamines and metanephrine.
114
What must be avoided before a 24-hour urine test for pheochromocytoma?
Coffee, tea, bananas, chocolate, vanilla, ASA, nicotine, amphetamines, and decongestants.
115
How does the Clonidine suppression test work?
In a normal individual, clonidine (an alpha-2 agonist) *blocks* catecholamine release. In a patient with a pheochromocytoma, it *fails* to suppress the release.
116
What is the crucial order of pharmacologic treatment *prior* to pheochromocytoma surgery?
Alpha blockade *must* be established *before* beta blockade. (e.g., Phentolamine or Phenoxybenzamine first, *then* a beta-blocker).
117
Why must alpha-blockade precede beta-blockade in pheochromocytoma management?
If beta-blockers (beta-2) are given first, it leaves alpha-1 stimulation unopposed, which can lead to severe, refractory hypertension.
118
What drugs are used for intraoperative BP control during pheochromocytoma removal?
Nitroprusside (for hypertension during tumor manipulation) and Phenylephrine (for hypotension after tumor ligation/removal).
119
What are the classic differences between IDDM (Type 1) and NIDDM (Type 2)?
IDDM: Thin, variable blood glucose, ketoacidosis common, requires insulin. NIDDM: Obese, stable blood glucose, ketoacidosis uncommon, does not always require insulin.
120
What are the '3 Polys' of diabetes?
Polyphagia (excessive hunger), Polydipsia (excessive thirst), and Polyuria (excessive urination).
121
What are the manifestations of *autonomic neuropathy* in diabetic patients?
Orthostatic hypotension, Resting tachycardia, Gastroparesis (vomiting, diarrhea), Impotence, Asymptomatic hypoglycemia, and Sudden death syndrome.
122
What are the signs and symptoms of Carcinoid Syndrome?
Cutaneous flushing, Labile (unstable) blood pressure, Diarrhea, Bronchospasm, and Cardiac failure (cardiomyopathy).
123
What is the treatment for Carcinoid Syndrome?
Fluid resuscitation, H1/H2 antagonists, Serotonin (5-HT) antagonists, Bronchodilators, Vasoactive drugs, and Octreotide.
124
What are the adverse responses to anesthesia in a hypothyroid
125
What are the adverse responses to anesthesia in a hypothyroid patient?
Sensitivity to depressant drugs (opioids), hypodynamic circulation, slowed drug metabolism, and impaired ventilatory responses.
126
What is the recommended anesthetic management for a severe hypothyroid patient?
Preoperative supplemental hydrocortisone, Induction (Ketamine is a good choice), Maintenance (ultrashort-acting drugs), and defer extubation until the patient is responsive and normothermic.
127
What are the signs of hypercalcemia?
Decreased GFR/kidney stones, Hypertension, prolonged P-R interval, *short* Q-T interval, peptic ulcers, pancreatitis, and bone demineralization.
128
What are the signs and symptoms of hypocalcemia?
Perioral paresthesia, restlessness, neuromuscular irritability (positive Chvostek or Trousseau sign), inspiratory stridor, and a *prolonged* Q-T interval.
129
What are the main fluid compartments and their key electrolytes?
Intracellular (2/3): High in Potassium (K+), Magnesium (Mg2+), and Phosphates. Extracellular (1/3): High in Sodium (Na+), Chloride (Cl-), and Bicarbonate (HCO3-).
130
What force controls fluid distribution between the interstitium and the intracellular compartment?
Osmotic forces alone.
131
What is the function of ADH (Antidiuretic Hormone)?
Released from the posterior pituitary, it causes the reabsorption of *water* (not salt) from the distal tubules and collecting ducts. Results in less, more concentrated urine.
132
What is the function of Aldosterone?
Released from the adrenal cortex, it causes renal tubules to increase the reabsorption of *sodium* (and water follows). Results in less urine.
133
What is the function of Natriuretic hormones (ANP, BNP)?
Produced in the heart/brain in response to stretch; they *cause sodium loss* in the kidneys (opposite of Aldosterone).
134
What is a sensitive measure of Extracellular Fluid Volume (ECV) deficit?
Sudden weight loss.
135
What is hyponatremia and what is a common cause?
Too little sodium per volume (concentration is too low, < 135 mEq/L). Often caused by *too much water* (e.g., SIADH) rather than too little salt.
136
What is hypernatremia and what is a common cause?
Too much sodium per volume (concentration is too high, > 145 mEq/L). Often caused by a *water deficit* (dehydration) rather than too much salt.
137
What are the four potential physiologic causes of Edema?
1. Increased capillary hydrostatic pressure, 2. Decreased capillary osmotic pressure (low albumin), 3. Increased interstitial osmotic pressure, 4. Blockage of lymph movement.
138
What is the normal extracellular K+ concentration?
Around 3.5 - 5.0 mEq/L. (Slide says 5, but 3.5-5 is standard).
139
How does hypokalemia (low K+) affect the resting membrane potential?
It *hyperpolarizes* the membrane (makes it more negative), leading to less likelihood of cellular activation (muscle weakness, slow heart rate).
140
How does hyperkalemia (high K+) affect the resting membrane potential?
It *hypopolarizes* the membrane (makes it less negative), leading to increased excitability initially, but then prevents repolarization (flaccid paralysis, cardiac arrest).
141
Hypomagnesemia can lead to what other electrolyte imbalance, which must be fixed first?
Hypokalemia. Magnesium is needed to replace potassium.
142
How does low magnesium (Hypomagnesemia) affect the neuromuscular junction (NMJ)?
Leads to *more* Acetylcholine (Ach) release and neuromuscular excitability (tetany, spasms).
143
How does high magnesium (Hypermagnesia) affect the neuromuscular junction (NMJ)?
Leads to *decreased* Acetylcholine (Ach) release (muscle weakness, respiratory depression).
144
What are the three main systems in the body that regulate acid-base balance?
1. Buffers (Bicarbonate, Phosphates), 2. Respiratory system (controls CO2), 3. Kidneys (control H+ and HCO3-).
145
What is the bicarbonate buffer system equation?
CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3-.
146
What is the difference between acidosis and acidemia?
Acidosis is a *process* that tries to make the blood more acidic. Acidemia is the *state* of the blood pH being low (e.g., pH < 7.35).
147
What are the lab findings and compensation for Metabolic Acidosis?
Labs: Low Bicarb (HCO3-). Compensation: Hyperventilation (to blow off CO2 and raise pH).
148
What are the lab findings and compensation for Respiratory Acidosis?
Labs: High CO2 (hypoventilation). Compensation: Renal excretion of acid (kidneys retain HCO3-).
149
What are the lab findings and compensation for Metabolic Alkalosis?
Labs: High Bicarb (HCO3-) (e.g., from vomiting or antacids). Compensation: Hypoventilation (to retain CO2 and lower pH).
150
What are the lab findings and compensation for Respiratory Alkalosis?
Labs: Low CO2 (hyperventilation). Compensation: Renal excretion of bicarb (kidneys dump HCO3-).
151
What is the most common endocrine disorder?
Diabetes mellitus.
152
What transporter does insulin trigger the insertion of, and in what tissues?
GLUT 4 transporters (slide says GLUT 2, but GLUT 4 is standard) in adipose and muscle cells.
153
What tissues do *not* require insulin for glucose uptake?
Nervous tissue (brain) and Red Blood Cells (RBCs).
154
What is Type 1 Diabetes Mellitus (T1DM)?
An autoimmune disease causing sudden, severe insulin deficiency due to the destruction of the beta cells in the islets of Langerhans.
155
Why does hyperglycemia occur in T1DM (two reasons)?
1. Lack of insulin prevents glucose from entering cells. 2. Unopposed glucagon secretion leads to gluconeogenesis and glycogenolysis (dumping more glucose into the blood).
156
Why does ketoacidosis occur in T1DM?
Cells are starving, so metabolism shifts to fat. Excessive breakdown of fatty acids produces ketone bodies (metabolic acids), which drop the blood pH.
157
What is the primary problem in Type 2 Diabetes (T2DM)?
Insulin resistance: Target tissues (muscle, adipose) become 'deaf' to insulin's effects.
158
What is the biggest predictor (risk factor) for T2DM?
Obesity (also aging and sedentary lifestyle).
159
Why is ketoacidosis rare in T2DM?
There is still *some* insulin present (at least initially), which is enough to keep lipolysis (fat breakdown) in check.
160
What severe complication is a frequent problem in T2DM?
Nonketotic hyperglycemic hyperosmolar coma (NHHC), resulting from rapid, severe dehydration.
161
Why does Gestational Diabetes Mellitus (GDM) occur?
Pregnant women need 2-3x the amount of insulin. GDM occurs when they cannot produce this much or they become resistant.
162
What are the most common problems associated with GDM?
Macrosomia (really big babies) and neonatal hypoglycemia (baby has been overproducing insulin to handle mom's high sugar).
163
What is 'Prediabetes'?
Having Impaired Fasting Glucose (IFG) and/or Impaired Glucose Tolerance (IGT).
164
What are the *macrovascular* effects of chronic hyperglycemia?
Heart disease and stroke (e.g., atherosclerosis).
165
What are the *microvascular* effects of chronic hyperglycemia?
Retinopathy (blindness) and Nephropathy (renal failure).
166
What are the *neural* effects of chronic hyperglycemia?
Autonomic neuropathy (GI, bladder, erectile dysfunction) and Sensory dysfunction (paresthesias, lack of sensation in feet).
167
How do Sulfonylureas (e.g., Glyburide) work?
They stimulate insulin secretion by binding to K-ATP channels in beta cells, causing depolarization and insulin release.
168
How does Metformin (a biguanide) work?
It suppresses hepatic (liver) glucose production and increases insulin sensitivity in target tissues. Does *not* typically cause hypoglycemia.
169
What are the general onsets/durations for Rapid-Acting, Intermediate-Acting, and Long-Acting insulins?
Rapid: Onset < 30 min, Peak ~2h, Duration < 5h. Intermediate: Onset ~2h, Peak ~11h, Duration ~24h. Long: Works slowly over 24h (no peak).
170
What is the most dangerous, acute problem associated with attempts to control blood sugar in T1DM?
Hypoglycemia.
171
What does monitoring Glycosylated Hemoglobin (HbA1c) tell you?
It provides an index of blood sugar control over the lifetime of an RBC (3-4 months) and doesn't change rapidly like a single blood glucose reading.
172
What is the standard method for patient self-monitoring of blood glucose?
Capillary blood glucose, using a glucose oxidase reagent test strip.
173
Microvascular vs. Macrovascular complications: which is more common in IDDM vs NIDDM?
Microvascular complications (retinopathy, nephropathy) predominate in IDDM. Macrovascular complications (heart disease, stroke) are more common in NIDDM.
174
How does diabetic autonomic neuropathy affect perioperative morbidity?
Perioperative morbidity is *increased* in diabetics with evidence of autonomic neuropathy.
175
What is the correlation for diabetic microangiopathy?
It correlates with the *degree and duration* of hyperglycemia.
176
What are the cardiovascular manifestations of diabetic autonomic neuropathy?
Orthostatic hypotension, resting tachycardia, and decreased or absent beat-to-beat heart rate variation.
177
How can diabetic autonomic neuropathy obscure ischemic heart disease?
It may prevent the development of angina pectoris, leading to a 'silent' or painless myocardial infarction.
178
What is gastroparesis and why is it an anesthetic concern?
A manifestation of autonomic neuropathy (delayed gastric emptying); it presents a high risk for pulmonary aspiration (may need RSI).
179
What is Stiff Joint Syndrome in diabetes and why is it an anesthetic concern?
Limited joint mobility (e.g., 'Prayer Sign') due to glycosylation of collagen; it can make laryngoscopy and intubation difficult.
180
How do volatile anesthetics affect insulin release?
They may *impair* the release of insulin in response to glucose administration.
181
Why is the administration of Lactated Ringer's (LR) controversial in diabetic patients?
Lactate is converted to glucose by the liver, which may increase the patient's insulin requirement.
182
What drug can be used for diabetic gastroparesis?
Metoclopramide (Reglan), which increases gastric motility.
Pathophysiology
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